The project undertakes genome-wide methylation analysis on patients’ primary and metastatic cancers to identify the different methylation patterns in each. The first investigative phase involves five patients, in whom CRC has spread to the lymph nodes. Tumour samples were taken during operations pre-scheduled as part of their personal cancer care programme, in which the tumours were surgically removed. Next generation sequencing techniques were used for the primary analysis and resulted in the identification of 94 genes which were hypermethylated in the lymph node tumours, as compared to the primary tumours. Ili says: ‘Of these, PUM1, MAGED1, ZNF655, DLEU7 and LIX1L genes presented differences of over 50 per cent in their methylation status, from the original adenocarcinoma.’ She explains: ‘We understand these particular genes to be involved in the regulation of cell cycles, stem cell differentiation and the regulation of micro RNA-mediated inhibition of translation.’ The implication is that hypermethylation of specific promoter regions of these genes could be the trigger for the metastasis of the original cancer. There are multiple steps behind metastasis and one of the main requirements is for epithelial cells forming the primary tumour to change character, becoming mesenchymal stem cells with the potential to change into multiple different types of cells. The tumour develops blood vessels into which these mesenchymal cells migrate and can thus flow through the body. At the secondary site, these cells pass across the vascular wall and begin to grow a metastatic tumour. Therefore, by their very nature these secondary tumours are considerably more aggressive, with greater migratory and proliferative characteristics than the former adenocarcinoma.